The receptor cells for acoustic stimuli are particularly vulnerable to reduced oxygen tension because of the limited characteristics of blood supply to the inner ear. Electrophysiological data have demonstrated that asphyxiation disrupts audition, but the consequences of mild, prolonged hyposia upon the auditory system have not been investigated. One aim of this investigation is to determine whether subchronic exposure to chemical asphyxiants at doses relevant to levels widely encountered in occupational and environmental settings produces ototoxicity. Chronic and impulse noise can induce autitory damage, but whether this occurs through mechanical trauma or by metabolic exhaustion is uncertain. Because there are data which show that noise reduces oxygen tension in the endolymph fluid of the scala media and produces vascular damage to the inner ear, it has been hypothesized that noise-induced auditory loss may result from depressed oxygen availability. If noise does disrupt hearing by restricting oxygen to the Corti Organ or if it damages inner ear vascular structures it is logical to assume that noise would potentiate the ototoxic effects of chemical asphyxiant exposure. The final aim of this proposal will be to specify the nature of the interaction between noise and chemical asphyxiant exposure. The methods to be used include measures of modulation of the acoustic startle reflex by low intensity test stimuli and subsequent histological examination of the inner ear.